Evolutionarily stable gene clusters shed light on the common grounds of pathogenicity in the Acinetobacter calcoaceticus-baumanniicomplex

Nosocomial pathogens of the Acinetobacter calcoaceticus-baumannii (ACB) complex are a cautionary example for the world-wide spread of multi- and pan-drug resistant bacteria. Aiding the urgent demand for novel therapeutic targets, comparative genomics studies between pathogens and their apathogenic relatives shed light on the genetic basis of human-pathogen interaction. Yet, existing studies are limited in taxonomic scope, sensing of the phylogenetic signal, and resolution by largely analyzing genes isolated from their functional contexts. Here, we explored more than 3,000 Acinetobacter genomes in a phylogenomic framework integrating orthology-based phylogenetic profiling and micro-synteny conservation analyses. This allowed to delineate gene clusters in the type strain A. baumannii ATCC 19606 whose evolutionary conservation indicates a functional integration of the subsumed genes. These evolutionarily stable gene clusters (ESGCs) reveal metabolic pathways, transcriptional regulators residing next to their targets but also tie together sub-clusters with distinct functions to form higher-order functional modules. We shortlisted 150 ESGCs that either co-emerged with, or are found preferentially in, the pathogenic ACB clade. They unveil, at an unprecedented resolution, the genetic makeup that coincides with the manifestation of the pathogenic phenotype in the last common ancestor of the ACB clade. Key innovations are the remodeling of the regulatory-effector cascade connecting LuxR/LuxI quorum sensing via an intermediate messenger to biofilm formation, the extension of micronutrient scavenging systems, and the increase of metabolic flexibility by exploiting carbon sources that are provided by the human host. Specifically, we could show that only members of the ACB clade use kynurenine as a sole carbon and energy source, a substance produced by humans to fine-tune the antimicrobial innate immune response. In summary, this study provides a rich and unbiased set of novel testable hypotheses on how pathogenic Acinetobacter interact with and ultimately infect their human host. They disclose promising routes for future therapeutic strategies.

The evolution of partner specificity in mutualisms

Mutualistic species vary in their level of partner specificity, which has important evolutionary, ecological, and management implications. Yet, the evolutionary mechanisms which underpin partner specificity are not fully understood. Most work on specialization focuses on the trade-off between generalism and specialism, where specialists receive more benefits from preferred partners at the expense of benefits from non-preferred partners, while generalists receive similar benefits from all partners. Because all mutualisms involve some degree of both cooperation and conflict between partners, we highlight that specialization to a mutualistic partner can be cooperative, increasing benefit to a focal species and a partner, or antagonistic, increasing resource extraction by a focal species from a partner. We devise an evolutionary game theoretic model to assess the evolutionary dynamics of cooperative specialization, antagonistic specialization, and generalism. Our model shows that cooperative specialization leads to bistability: stable equilibria with a specialist host and its preferred partner excluding all others. We also show that under cooperative specialization with spatial effects, generalists can thrive at the boundaries between differing specialist patches. Under antagonistic specialization, generalism is evolutionarily stable. We provide predictions for how a cooperation-antagonism continuum may determine the patterns of partner specificity that develop within mutualistic relationships.

Best Reply Player Against Mixed Evolutionarily Stable Strategy User

We consider matrix games with two phenotypes (players): one following a mixed evolutionarily stable strategy and another one that always plays a best reply against the action played by its opponent in the previous round (best reply player, BR). We focus on iterated games and well-mixed games with repetition (that is, the mean number of repetitions is positive, but not infinite). In both interaction schemes, there are conditions on the payoff matrix guaranteeing that the best reply player can replace the mixed ESS player. This is possible because best reply players in pairs, individually following their own selfish strategies, develop cycles where the bigger payoff can compensate their disadvantage compared with the ESS players. Well-mixed interaction is one of the basic assumptions of classical evolutionary matrix game theory. However, if the players repeat the game with certain probability, then they can react to their opponents’ behavior. Our main result is that the classical mixed ESS loses its general stability in the well-mixed population games with repetition in the sense that it can happen to be overrun by the BR player.

Ecological memory preserves phage resistance mechanisms in bacteria

Bacterial defenses against phage, which include CRISPR-mediated immunity and other mechanisms, can carry substantial growth rate costs and can be rapidly lost when pathogens are eliminated. How bacteria preserve their molecular defenses despite their costs, in the face of variable pathogen levels and inter-strain competition, remains a major unsolved problem in evolutionary biology. Here, we present a multilevel model that incorporates biophysics of molecular binding, host-pathogen population dynamics, and ecological dynamics across a large number of independent territories. Using techniques of game theory and non-linear dynamical systems, we show that by maintaining a non-zero failure rate of defenses, hosts sustain sufficient levels of pathogen within an ecology to select against loss of the defense. This resistance switching strategy is evolutionarily stable, and provides a powerful evolutionary mechanism that maintains host-pathogen interactions, selects against cheater strains that avoid the costs of immunity, and enables co-evolutionary dynamics in a wide range of systems.

Animism and Language Evolution

The exact mechanism of the evolution of language remains unknown. One of the central problems in this field is the issue of reliability and deceit that can be characterized in terms of honest signaling theory. Communication systems become vulnerable to dishonesty and deceit when there are conflicting interests between the signaler and receiver. The handicap principle explains how evolution can prevent animals from deceiving each other even if they have a strong incentive to do so. It suggests that the signals must be costly in order to provide accurate and reliable communication between animals. Language-like communication systems, being inherently vulnerable to deception, could only evolve and become evolutionarily stable if they had some mechanisms that can make the communication hard to fake and trustworthy. One of the theories that try to solve the problem of reliability and deception is the ritual/speech coevolution hypothesis. According to this theory, hard-to-fake rituals evolved concurrently with language - by reinforcing trust and solidarity among early humans and preventing deceitful and manipulative behavior within the group. One of the drawbacks of this hypothesis is that the relationship between ritual and speech is too indirect. Rituals could not have a real-time effect on every instance of speech and encompass all aspects of everyday language communication. Therefore they are not efficient enough to provide instant verification mechanisms to guarantee honest communication. It is more likely that the animistic nature of language itself, rather than ritual, was the handicap-like cost that helped to ensure the reliability of language during its origin. The belief in the parallel dimension of animistic spirits emerged concurrently with language as a hard-to-fake attestation mechanism that ensured inviolability of one's speech. The notion that animism emerged because of early behaviorally modern humans’ incoherent and flawed observations about the natural world is unlikely, because it implies a very improbable scenario, that there had been a more coherent and rational pre-animistic period which later degraded to animistic one.

DNA damage repair system in C57BL/6 J mice is evolutionarily stable

Background DNA damage repair (DDR) system is vital in maintaining genome stability and survival. DDR consists of over 160 genes in 7 different pathways to repair specific type of DNA damage caused by external and internal damaging factors. The functional importance of DDR system implies that evolution could play important roles in maintaining its functional intactness to perform its function. Indeed, it has been observed that positive selection is present in BRCA1 and BRCA2 (BRCA), which are key genes in homologous recombination pathway of DDR system, in the humans and its close relatives of chimpanzee and bonobos. Efforts have been made to investigate whether the same selection could exist for BRCA in other mammals but found no evidence so far. However, as most of the studies in non-human mammals analyzed only a single or few individuals in the studied species, the observation may not reflect the true status in the given species. Furthermore, few studies have studied evolution selection in other DDR genes except BRCA. In current study, we used laboratory mouse C57BL/6 J as a model to address evolution selection on DDR genes in non-primate mammals by dynamically monitoring genetic variation across 30 generations in C57BL/6 J. Results Using exome sequencing, we collected coding sequences of 169 DDR genes from 44 C57BL/6 J individual genomes in 2018. We compared the coding sequences with the mouse reference genome sequences derived from 1998 C57BL/6 J DNA, and with the mouse Eve6B reference genome sequences derived from 2003 C57BL/6 J DNA, covering 30 generations of C57BL/6 J from 1998 to 2018. We didn’t identify meaningful coding variation in either Brca1 or Brca2, or in 167 other DDR genes across the 30 generations. In the meantime, we did identify 812 coding variants in 116 non-DNA damage repair genes during the same period, which served as a quality control to validate the reliability of our analytic pipeline and the negative results in DDR genes. Conclusions DDR genes in laboratory mouse strain C57BL/6 J were not under positive selection across its 30-generation period, highlighting the possibility that DDR system in rodents could be evolutionarily stable.

Cultural diversity and wisdom of crowds are mutually beneficial and evolutionarily stable

The ability to learn from others (social learning) is often deemed a cause of human species success. But if social learning is indeed more efficient (whether less costly or more accurate) than individual learning, it raises the question of why would anyone engage in individual information seeking, which is a necessary condition for social learning’s efficacy. We propose an evolutionary model solving this paradox, provided agents (i) aim not only at information quality but also vie for audience and prestige, and (ii) do not only value accuracy but also reward originality—allowing them to alleviate herding effects. We find that under some conditions (large enough success rate of informed agents and intermediate taste for popularity), both social learning’s higher accuracy and the taste for original opinions are evolutionarily-stable, within a mutually beneficial division of labour-like equilibrium. When such conditions are not met, the system most often converges towards mutually detrimental equilibria.

Allelopathy as an evolutionarily stable strategy

In plants, most competition is resource competition, where one plant simply pre-empts the resources away from its neighbours. Interference competition, as the name implies, is a form of direct interference to prevent resource access. Interference competition is common among animals who can physically fight, but in plants, one of the main mechanisms of interference competition is Allelopathy. allelopathic plants release of cytotoxic chemicals into the environment which can increase their ability to compete with surrounding organisms for limited resources. The circumstances and conditions favoring the development and maintenance of allelochemicals, however, is not well understood. Particularly, it seems strange that, despite the obvious benefits of allelopathy, it seems to have only rarely evolved. To gain insight into the cost and benefit of allelopathy, we have developed a 2x2 matrix game to model the interaction between plants that produce allelochemicals and plants that do not. Production of an allelochemical introduces novel cost associated with synthesis and detoxifying a toxic chemical but may also convey a competitive advantage. A plant that does not produce an allelochemical will suffer the cost of encountering one. Our model predicts three cases in which the evolutionarily stable strategies are different. In the first, the non-allelopathic plant is a stronger competitor, and not producing allelochemicals is the evolutionarily stable strategy. In the second, the allelopathic plant is the better competitor and production of allelochemicals is the more beneficial strategy. In the last case, neither is the evolutionarily stable strategy. Instead, there are alternating stable states, depending on whether the allelopathic or non-allelopathic plant arrived first. The generated model reveals circumstances leading to the evolution of allelochemicals and sheds light on utilizing allelochemicals as part of weed management strategies. In particular, the wide region of alternative stable states in most parameterizations, combined with the fact that the absence of allelopathy is likely the ancestral state, provides an elegant answer to the question of why allelopathy rarely evolves despite its obvious benefits. Allelopathic plants can indeed outcompete non-allelopathic plants, but this benefit is simply not great enough to allow them to go to fixation and spread through the population. Thus, most populations would remain purely non-allelopathic.